1. Subarachnoid Haemorrhage

2. SAH SAH What is it? What is it? –Bleeding into the subarachnoid space (space between the pia & arachnoid meningeal layers) where blood vessels lie & CSF flows Where does the blood come from? Where does the blood come from? –An aneursym on a blood vessel in the subarachnoid space has ruptured (~70%) –Unknown (~15%) –AVM (~10%) –Rare causes (e.g. tumour) (~5%) Where does the blood go? Where does the blood go? –Anywhere where CSF goes, may get hydrocephalus if into ventricle & causes obstruction of CSF circulation

3. SAH Incidence = 1/7000 people Incidence = 1/7000 people Higher chance if: Higher chance if: –Female –3 rd trimester of pregnancy –Middle-aged –Abuse of stimulant drugs –Connective tissue disorder –Family history –PCKD

4. What causes aneurysms to form? Defects in the media of the arteries Defects in the media of the arteries Defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations Defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations

5. What causes aneurysms to rupture? The probability of rupture is related to the tension on the aneurysm wall The probability of rupture is related to the tension on the aneurysm wall The law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm The law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm Therefore, the rate of rupture is directly related to the size of the aneurysm Therefore, the rate of rupture is directly related to the size of the aneurysm Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosis Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosis

6. SAH – The Problem They occur in young people They occur in young people –80% in 40-65 year olds –15% in 20-40 year olds It can kill quickly It can kill quickly –25% die within 24 hours –50% will be dead at 6 months It causes significant disability It causes significant disability –Cognitive impairment –Neurological disability depending on size of bleed & complications encountered

7. How do they present? Headache Headache –sudden onset & severe –small leak may cause minor headache & may be warning sign of rupture Reduced consciousness Reduced consciousness Meningism Meningism –Vomiting –Neck stiffness –Photophobia Seizures Seizures

8. What causes symptoms & signs? Blood leaking from the aneurysm Blood leaking from the aneurysm Local pressure effects of the aneurysm Local pressure effects of the aneurysm Associated ICH Associated ICH Emboli Emboli

9. What causes symptoms & signs? Blood leaking from the aneurysm Blood leaking from the aneurysm –Headache –Meningism

10. What causes symptoms & signs? Local pressure effects of the aneurysm Local pressure effects of the aneurysm –Acom Visual symptoms due to optic chiasm compression Visual symptoms due to optic chiasm compression Positive babinski Positive babinski Bilateral lower limb paresis Bilateral lower limb paresis –MCA Contralateral hand & face paresis Contralateral hand & face paresis Contralateral visual neglect Contralateral visual neglect Aphasia (dominant side) Aphasia (dominant side) –ICA/Pcom CNIII signs CNIII signs

11. What causes symptoms & signs? Associated ICH Associated ICH –The aneurysm usually lies within the subarachnoid cisterns –It can become adherent to adjacent brain due to adhesions (e.g. from a previous leak) –The bleed therefore can also extend into the brain MCA = TL causing hemiparesis & aphasia (if dominant) MCA = TL causing hemiparesis & aphasia (if dominant) Acom = mutism Acom = mutism –AVM is more likely to cause ICH as they usually lie somewhat in brain parenchyma

12. Headache A sudden onset severe headache IS caused by a SAH until you have done investigations which prove otherwise A sudden onset severe headache IS caused by a SAH until you have done investigations which prove otherwise

13. Sudden onset severe headache

16. Investigations CT scan without contrast CT scan without contrast Lumbar puncture Lumbar puncture CT COW CT COW Cerebral angiogram Cerebral angiogram MRI/MRA MRI/MRA 98% sensitive @ 12 hours 80% at day 3 50% at day 7 Also good to see if any associated ICH or hydrocephalus. May help localise the location of the aneurysm if there is more than 1 & may also see AVM

17. Where is the aneurysm? Where is the blood on the CT scan? – –Basal cisterns – COW aneurysm – –Sylvian fissure – ICA, Pcom, MCA – –Interhemispheric or intraparenchymal - Acom

24. A cistern where the arachnoid extends across between the two temporal lobes, and encloses the cerebral peduncles including the structures contained in the interpeduncular fossa.cistern temporal lobescerebral pedunclesinterpeduncular fossa MCA stroke - Emergency neuroradiology. Axial CT scan at the level of the basal cisterns shows the "hyperdense middle cerebral artery (MCA) sign" (arrow) representing acute clot within the right middle cerebral artery, accounting for the patient's clinical symptoms

25. SAH & LP CT & LP are critical to diagnosing SAH No need for LP if obvious blood in subarachnoid space on CT Blood may not be evident on CT, especially if it is performed > few days after bleed LP should only be performed after 12 hours of headache onset

26. SAH & LP When blood enters the CSF (e.g. from SAH or during LP) the red cells are broken down & oxyhaemoglobin is released It then takes 12 hours for the oxyhaemoglobin to be converted into bilirubin – conversion is via an enzyme found in the brain. Bilirubin in the CSF, therefore, tells us that blood must have been in the subarachnoid space for at least 12 hours Blood which entered the CSF during the LP would not encounter the enzyme & could not produce bilirubin The CSF will look xanthochromic (yellowish discolouration) if bilirubin is present which they will look for with spectroscopy in the lab

27. What may I find on examination? Normal exam Normal exam Confusion/memory loss Confusion/memory loss Aphasia Aphasia CN abnormalites CN abnormalites –CNII – papilloedema, usually mild initially & retinal haemorrhages –CNIII – palsy Hemiparesis/neglect Hemiparesis/neglect Obs – HTN, tachycardic, febrile Obs – HTN, tachycardic, febrile

28. Treatment Main aim is damage control – want to prevent further bleeding & try to avoid the complications that SAH patients get Main aim is damage control – want to prevent further bleeding & try to avoid the complications that SAH patients get SAH patients will vary greatly from GCS 15/15 to GCS 3/15 SAH patients will vary greatly from GCS 15/15 to GCS 3/15

30. To coil or clip? Coiling – –Endovascular technique done in angiography by interventional radiologists under GA – –May be best if small necked aneurysm – –Used in particularly sensitive areas e.g. basilar tip – –Must be able to access the aneurysm (e.g. any stenosis or tortuous vessels) – –Like dome:neck ratio to be 2:1 or greater Clipping –Craniotomy & careful dissection using microscope to reach aneurysm & clip usually at neck –May be performed after failed clipping –If aneurysm can’t be reached by the endovascular root

31. That’s Dandy First to clip an aneursym successfully in 1937 First to clip an aneursym successfully in 1937 Walter Dandy Walter Dandy

32. Operative microscope

33. Complications with SAH 1. Re-bleeding 2. Hydrocephalus 3. Vasospasm 4. Hyponatraemia 5. Seizures 6. VTE

34. Complications with SAH Re-bleeding Re-bleeding –80% mortality if re-bleed –Greatest risk is in the first 24 hours after the initial bleed –Aim to prevent by controlling BP to avoid dramatic changes & isolate the aneurysm from the circulation (coil or clip)

35. Complications with SAH Hydrocephalus – –Obstructive Blood enters the ventricles & can block the flow of CSF e.g. at the aqueduct or outlet of the 4 th ventricle – –Communicating Due to blood blocking reabsorption of CSF through the arachnoid granules – –May need an extraventricular drain to treat – –Keep head of bed at 30 0 (promote CSF flow & venous return)

36. Complications with SAH Vasospasm – –Blood vessel goes into spasm causing ischaemia - stroke – –To prevent keep them filled with at least 3L fluid day & nimodipine IV/PO & insert central line to monitor central venous pressure – aiming for 8-10 – –Suspected with deteriorating GCS/new neurological deficit – –Treatment – Urgent CT brain to rule out a bleed as a cause of the deterioration then urgent angiogram to diagnose & treat vasospasm – –Greatest risk of vasospasm is days 4-7 but significant risk for first 3 weeks after bleed, therefore will use preventative measures for at least 3 weeks

37. Complications with SAH Hyponatraemia – –Susceptible due to being fluid loaded & cerebral salt wasting – –Cerebral salt wasting = renal loss of sodium due to intracranial pathology ? Cause. Loss of water & salt (whereas SIADH is loss of salt & retention of water) – –Treat with normal or hypertonic saline – –If refractory may need a mineralocorticoid e.g. fludrocortisone to stimulate renal reabsorption – but this should only be used under instructions from consultant endocrinologist

38. Complications with SAH Seizures – –A seizure is a disturbance of sensation, movement or consciousness – –All seizures originate from the surface of the brain – cortex – –Blood is an irritant to the cortex – –Prophylaxis with phenytoin or levetiracetam – –Ensure phenytoin levels are therapeutic – –Treat as seizure from any cause & suspect re-bleed

39. Complications with SAH VTE – –On bed rest – –TEDS – –Prophylactic enoxaparin as soon as consultant sees fit – –Always keep VTE in the back of your mind

40. How are SAH graded? GCS 15, only CN deficit if any Grade 1 No blood GCS 13-14, no deficit Grade 2 Diffuse blood, no clots & <1mm GCS 13-14, with deficit Grade 3 Clots & blood 1mm or more GCS 7-12, +/- deficit Grade 4 ICH or intraventricular clots GCS 3-6 +/- deficit Grade 5 World Federation Neurosurgeons Fischer grading

41. Subdural Haematoma

42. Extra-dural haematoma

43. Extra-dural haemtoma

44. Intra-parenchymal haematoma